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Table 2 Summary of the major characteristic molecular features of PMLBCL

From: Novel drug targets for personalized precision medicine in relapsed/refractory diffuse large B-cell lymphoma: a comprehensive review

Genetic Aberration: Gain of function

Genetic Aberration: Loss of function

Pathways: Upregulated/Gain

Pathways: Inhibited/Loss

Study

JAK2 (9p24.1 Ampl)

SOCS1 (Mut)

JAK/STAT (STAT1, STAT3, STAT6) c-MYC PD-1/PD-L1/2

 

[57, 60, 603–605]

STAT6 (Mut)

PTPN1 (Mut)

STAT6

PTPN1

[558, 606]

JMJD2C (9p24.1 Ampl)

 

c-MYC

 

[603]

CD274 (PD-L1) (Tx/ 9p24.1Ampl) PDCD1LG2 (PD-L2) (Tx/Ampl)

 

PD-1

 

[607, 608]

 

TNFAIP3 (A20) (Mut)

NF-κB (c-REL), TRAF1

A20

[56, 609]

 

CIITA (Tx)

PD-1

HLA II complex

[64, 610]

 

TP53 (Mut)

 

TP53

[611]

  1. Overlapping molecular features of PMLBCL and ABC-DLBCL are marked as italic. Overlapping molecular features of PMLBCL, GCB-DLBCL and ABC-DLBCL are marked as bold. Normal letters refer to genetic aberrations that contribute to DLBCL pathogenesis, regardless of subtype.
  2. DLBCL diffuse large B cell lymphoma, ABC activated B cell-like, GCB germinal center B cell-like, PMLBCL primary mediastinal (thymic) large B-cell lymphomas, Del deleted/deletions, Mut mutated/mutations, Ampl amplified/amplification, Tx translocations, PRDM1/BLIMP1 B lymphocyte-induced maturation protein 1, PD-L1/L2 programmed cell death ligand 1/2, JMJD2C jumonji domain containing 2c, PTPN1 phosphotyrosine phosphatase N1, SOCS1 suppressor of cytokine signaling 1, TNFAIP3 tumor necrosis factor, alpha-induced protein, 3, NF-κB nuclear factor-kappa B, TRAF TNF receptor-associated factor, STAT signal transducer and activator of transcription, HLA human leukocyte antigens
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Molecular Cancer

ISSN: 1476-4598